Prevalence of anal squamous intra-epithelial lesion in women presenting genital squamous intra-epithelial lesion.

OBJECTIVE: To determine the frequency of anal squamous intra-epithelial lesions (ASIL) in women with genital squamous intra-epithelial lesions (GSIL). STUDY DESIGN: In a cross sectional study, 184 patients with histopathological diagnosis of GSIL and 76 controls without GSIL, were submitted to anuscopy in order to determine the presence of ASIL. All the women were HIV-negative with anal aceto-white lesions were biopsed for histological diagnosis. RESULTS: The frequency of ASIL was 17.4% in the GSIL group (3.2% high grade ASIL) and only 2.6% in the control group (0% high grade ASIL) (p<0.001). All the high grade ASIL diagnoses were found in women with cervical SIL. CONCLUSION: Women presenting GSIL have high prevalence of ASIL.

Vulvar intraepithelial neoplasia p53 expression, p53 gene mutation and HPV in recurrent/progressive cases.

OBJECTIVE: To evaluate p53 protein overexpression and p53 gene mutation in primary and recurrent undifferentiated vulvar intraepithelial neoplasia (VIN), establishing the recurrence and progression rates, median time interval, and sites of the initial lesion and first recurrence, addressing the relationship with HPV infection. STUDY DESIGN: Twenty women with undifferentiated VIN treated with wide surgical excision were followed every 6 months for 7 years and divided into groups with and without recurrence/progression. p53 Protein was detected in paraffin sections using the monoclonal p53 antibody. DNA was extracted from paraffin sections. Polymerase chain reaction/single strand conformation polymorphism (PCR-SSCP) analysis was utilized to screen for p53 gene mutations in exons 5-8. HPV was determined by digesting PCR products with restriction endonucleases. RESULTS: Recurrences were observed in 8 (40%) patients and progression to cancer in 1 (5%). Two cases recurred twice. The median interval for recurrence/progression was 24.5 months. Recurrent/progressive lesions were located in the same area of the initial lesions in 10 cases (91%). p53 Overexpression was observed in 50% (10/20) of primary lesions, of which 45% corresponded to the 9 recurrent/progressive cases. p53 Overexpression was detected in 81.8% (9/11) of recurrent/progressive cases. In the last 2 cases PCR-SSCP showed p53 gene mutation. The rate of HPV infection was higher in the group without recurrence. CONCLUSION: p53 Gene mutation plays an important role in undifferentiated VIN pathogenesis independent of high-risk HPV infection and may predict recurrence or progression to vulvar cancer. Undifferentiated VIN recurrent/progressive VIN lesions have a tendency to occur in the same area of the initial lesions, suggesting a molecular disturbance.

Human papillomavirus, Epstein-Barr virus and p53 mutation in vulvar intraepithelial neoplasia.

OBJECTIVE: To clarify the role of human papillomavirus (HPV) and Epstein-Barr virus (EBV) infection in vulvar carcinogenesis in relation to the mutated p53 gene. STUDY DESIGN: Polymerase chain reaction (PCR) was used to amplify DNA sequences of the viruses and PCR-single-strand conformation polymorphism analysis to screen for p53 gene mutations in exons 5-8 from formalin-fixed, paraffin-embedded blocks including 10 undifferentiated vulvar intraepithelial neoplasia (VIN) specimens. RESULTS: HPV and EBV DNA was found in 75% (6/8) and 0% (0/10) of VIN tissues, respectively. Oncogenic HPV 16 was the predominant type. HPV DNA extraction was not possible in 2 VIN specimens. p53 Gene mutation was shown in 20% (2/10) of VIN lesions. No correlation was found between p53 gene mutation the presence of viral HPV or EBV DNA. Mutated p53 was equally distributed between HPV-positive and -negative VIN cases. CONCLUSION: Our results suggest that although most undifferentiated VIN lesions are associated with HPV infection, p53 mutations may occur independent of viral infection even in the presence of oncogenic HPV. HPV, but not EBV or p53 gene mutation, can play a role in the pathogenesis of undifferentiated VIN.